Inhibition of HIV-1 replication by GB virus C infection through increases in RANTES, MlP-lα, MIP-1β, and SDF-1

@article{Xiang2004InhibitionOH,
  title={Inhibition of HIV-1 replication by GB virus C infection through increases in RANTES, MlP-l$\alpha$, MIP-1$\beta$, and SDF-1},
  author={Jinhua Xiang and Sarah L. George and Sabina W{\"u}nschmann and Qing Chang and Donna Klinzman and Jack T. Stapleton},
  journal={The Lancet},
  year={2004},
  volume={363},
  pages={2040-2046}
}
GBV-C viremia is associated with reduced CD4 expansion in HIV-infected people receiving HAART and interleukin-2 therapy
TLDR
GBV-C viremia was associated with a block in CD4 cell expansion following IL-2 therapy in the ACTG 328 study, and GBV- C status may be an important factor in IL- 2 treatment response.
GB virus C coinfection in advanced HIV type-1 disease is associated with low CCR5 and CXCR4 surface expression on CD4+ T-cells
TLDR
GBV-C coinfection in HIV-1 disease leads to reduced expression of the two major HIV- 1 coreceptors, CCR5 and CXCR4, on CD4(+) T-cells in patients at an advanced stage of immunodeficiency, providing a possible molecular explanation for the clinical benefit of GBV- C coinfections in late-stage HIV-2 disease.
Activation of Interferon Response Genes and of Plasmacytoid Dendritic Cells in HIV-1 Positive Subjects with GB Virus C Co-Infection
TLDR
Data indicate that in HIV-positive patients GBV-C coinfection promotes the activation of IFN-γ and downstream IRG expression, as well as with the activation/maturation of circulating pDC, and this crosstalk may suggest a role for GBv-C Coinfection in boosting the innate antiviral response to HIV infection.
GB virus type C infection modulates T-cell activation independently of HIV-1 viral load
TLDR
The association between GBV-C replication and lower T-cell activation may be a key mechanism involved in the protection conferred by this virus against HIV-1 disease progression to immunodeficiency in HIV- 1-infected patients.
Influence of GB virus C on IFN-γ and IL-2 production and CD38 expression in T lymphocytes from chronically HIV-infected and HIV-HCV-co-infected patients.
TLDR
The results suggest that neither GBV-C viremia nor the presence of E2 antibodies influence HIV and HCV viral replication or CD4 T cell counts in chronically infected patients and demonstrate that this effect may not be present in chronic infected patients, who represent the majority of patients in outpatient clinics.
GB virus type C E2 protein inhibits human immunodeficiency virus type 1 assembly through interference with HIV-1 gag plasma membrane targeting.
TLDR
Light is shed on a novel mechanism used by GBV-C E2 to inhibit HIV-1 replication and may provide insight into new approaches for suppressing HIV- 1 replication.
Postgenomic up-regulation of CCL3L1 expression in HTLV-2-infected persons curtails HIV-1 replication.
TLDR
A crucial protective role of CCL3L1 is confirmed from both HIV infection and disease progression, highlighting a previously not described functional up-regulation of this chemokine variant in both HIV-positive and -negative persons infected with HTLV-2.
Successful HAART is associated with high B-chemokine levels in chronic HIV type 1-infected patients.
TLDR
Successfully treated patients were able to produce higher amounts of beta-chemokines and normalize the coreceptor overexpression on T cells and may have clinical implications, such as a new strategy of using chemokines as adjuvants in anti-HIV therapy.
GB Virus C Infection Is Associated with Altered Lymphocyte Subset Distribution and Reduced T Cell Activation and Proliferation in HIV-Infected Individuals
TLDR
GBV-C infection was associated with reduced activation of CD4+ and CD8+ T cells in both HIV viremic and HIV RNA suppressed patients, and since cART therapy does not reduce T cell activation to levels seen in HIV-uninfected people, GBV- C infection may be beneficial for HIV-related diseases in those effectively treated with anti-HIV therapy.
Inhibition of HIV type 1 replication by human T lymphotropic virus types 1 and 2 Tax proteins in vitro.
TLDR
The contention that Tax1 and Tax2 play a role in generating antiviral responses against HIV-1 in vivo and in vitro is supported.
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